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[PMID]:28467275
[Au] Autor:Dos Santos PF; Mansur DS
[Ad] Endereço:Departament of Microbiology, Immunology and Parasitology, Centro de Ciências Biológicas, Universidade Federal de Santa Catarina , Santa Catarina, Brazil .
[Ti] Título:Beyond ISGlylation: Functions of Free Intracellular and Extracellular ISG15.
[So] Source:J Interferon Cytokine Res;37(6):246-253, 2017 Jun.
[Is] ISSN:1557-7465
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:ISG15 is a ubiquitin-like type I IFN-stimulated protein of 15 kDa and is one of the most prominently expressed proteins in viral infections. ISG15 is widely known to be involved in a process called ISGylation, where it binds to over 150 targets from a variety of classes of proteins including central immune signaling pathways such as those mediated by NFκB, JNK, and IRF-3. However, ISG15 also exists in a free form that can act intra- or extracellularly. In vitro and in vivo evidences suggest that free ISG15 play different roles in several cellular processes, from cancer and defense against viral infections to activation of immune cells such as lymphocytes, monocytes, and NK cells. This review discusses the roles of free intracellular and secreted ISG15 approaching questions yet to be answered about the mechanism of action of this protein.
[Mh] Termos MeSH primário: Infecções Bacterianas/imunologia
Citocinas/imunologia
Interferon gama/imunologia
Transdução de Sinais/imunologia
Ubiquitinas/imunologia
Viroses/imunologia
[Mh] Termos MeSH secundário: Infecções Bacterianas/genética
Infecções Bacterianas/microbiologia
Citocinas/genética
Regulação da Expressão Gênica
Seres Humanos
Fator Regulador 3 de Interferon/genética
Fator Regulador 3 de Interferon/imunologia
Interferon Tipo I/genética
Interferon Tipo I/imunologia
Interferon gama/genética
Monócitos/imunologia
Monócitos/microbiologia
Monócitos/virologia
Neutrófilos/imunologia
Neutrófilos/microbiologia
Neutrófilos/virologia
Linfócitos T/imunologia
Linfócitos T/microbiologia
Linfócitos T/virologia
Ubiquitinas/genética
Viroses/genética
Viroses/virologia
eIF-2 Quinase/genética
eIF-2 Quinase/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Cytokines); 0 (IRF3 protein, human); 0 (Interferon Regulatory Factor-3); 0 (Interferon Type I); 0 (Ubiquitins); 60267-61-0 (ISG15 protein, human); 82115-62-6 (Interferon-gamma); EC 2.7.11.1 (eIF-2 Kinase)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170504
[St] Status:MEDLINE
[do] DOI:10.1089/jir.2016.0103


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[PMID]:29295985
[Au] Autor:Conrad C; Di Domizio J; Mylonas A; Belkhodja C; Demaria O; Navarini AA; Lapointe AK; French LE; Vernez M; Gilliet M
[Ad] Endereço:Department of Dermatology, University Hospital CHUV, Lausanne, 1011, Switzerland. curdin.conrad@chuv.ch.
[Ti] Título:TNF blockade induces a dysregulated type I interferon response without autoimmunity in paradoxical psoriasis.
[So] Source:Nat Commun;9(1):25, 2018 01 02.
[Is] ISSN:2041-1723
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Although anti-tumor necrosis factor (TNF) agents are highly effective in the treatment of psoriasis, 2-5% of treated patients develop psoriasis-like skin lesions called paradoxical psoriasis. The pathogenesis of this side effect and its distinction from classical psoriasis remain unknown. Here we show that skin lesions from patients with paradoxical psoriasis are characterized by a selective overexpression of type I interferons, dermal accumulation of plasmacytoid dendritic cells (pDC), and reduced T-cell numbers, when compared to classical psoriasis. Anti-TNF treatment prolongs type I interferon production by pDCs through inhibition of their maturation. The resulting type I interferon overexpression is responsible for the skin phenotype of paradoxical psoriasis, which, unlike classical psoriasis, is independent of T cells. These findings indicate that paradoxical psoriasis represents an ongoing overactive innate inflammatory process, driven by pDC-derived type I interferon that does not lead to T-cell autoimmunity.
[Mh] Termos MeSH primário: Anticorpos Monoclonais/imunologia
Autoimunidade/imunologia
Interferon Tipo I/imunologia
Psoríase/imunologia
Fator de Necrose Tumoral alfa/imunologia
[Mh] Termos MeSH secundário: Adalimumab/efeitos adversos
Adalimumab/imunologia
Adalimumab/uso terapêutico
Adolescente
Adulto
Idoso
Animais
Anticorpos Monoclonais/efeitos adversos
Anticorpos Monoclonais/uso terapêutico
Autoimunidade/efeitos dos fármacos
Células Cultivadas
Doença de Crohn/tratamento farmacológico
Doença de Crohn/imunologia
Doença de Crohn/metabolismo
Citocinas/genética
Citocinas/imunologia
Citocinas/metabolismo
Células Dendríticas/efeitos dos fármacos
Células Dendríticas/imunologia
Células Dendríticas/metabolismo
Feminino
Seres Humanos
Infliximab/efeitos adversos
Infliximab/imunologia
Infliximab/uso terapêutico
Interferon Tipo I/genética
Interferon Tipo I/metabolismo
Masculino
Camundongos Endogâmicos BALB C
Meia-Idade
Psoríase/induzido quimicamente
Linfócitos T/efeitos dos fármacos
Linfócitos T/imunologia
Linfócitos T/metabolismo
Fator de Necrose Tumoral alfa/antagonistas & inibidores
Fator de Necrose Tumoral alfa/metabolismo
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antibodies, Monoclonal); 0 (Cytokines); 0 (Interferon Type I); 0 (Tumor Necrosis Factor-alpha); B72HH48FLU (Infliximab); FYS6T7F842 (Adalimumab)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180305
[Lr] Data última revisão:
180305
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180104
[St] Status:MEDLINE
[do] DOI:10.1038/s41467-017-02466-4


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[PMID]:29339070
[Au] Autor:Wang R; Li Y; Zhou Z; Liu Q; Zeng L; Xiao T
[Ad] Endereço:Hunan Engineering Technology Research Center of Featured Aquatic Resources Utilization, Hunan Agricultural University, Changsha 410128, China; College of Life and Environment Sciences, Hunan University of Arts and Science, Changde, Hunan 415000, China.
[Ti] Título:Involvement of interferon regulatory factor 3 from the barbel chub Squaliobarbus curriculus in the immune response against grass carp reovirus.
[So] Source:Gene;648:5-11, 2018 Mar 30.
[Is] ISSN:1879-0038
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:The barbel chub Squaliobarbus curriculus is an important commercial fish species in China, and has shown significant resistance to grass carp reovirus (GCRV). In this study, the cDNA sequence of interferon regulatory factors 3 (IRF3) from Squaliobarbus curriculus, designated as ScIRF3, was cloned, and its effect against GCRV was investigated. The full-length 1837 base pair (bp) cDNA of ScIRF3 contained a complete open reading frame of 1374 bp and encoded a putative polypeptide of 457 amino acid residues. The ScIRF3 protein contained conserved domains, including an N-terminal DNA-binding domain, a C-terminal IRF association domain, and a serine-rich domain. Phylogenetic analysis showed that ScIRF3 was closely clustered with IRF3s from Carassius auratus and Ctenopharyngodon idellus. Quantitative real-time polymerase chain reaction analysis showed that the expression levels of ScIRF3 in Squaliobarbus curriculus were the highest in the spleen and lowest in the muscle. After GCRV infection, expression levels of both ScIRF3 and type I interferon (IFN) were initially up-regulated and subsequently down-regulated in the spleen and intestine. Correlation analysis showed that the expression level of type I IFN is significantly positively correlated with that of ScIRF3 (Pearson correlation coefficient: 0.883, P: 0.004) in the intestine. The expression level of type I IFN was also significantly up-regulated and the GCRV titer was significantly decreased (P < .05) in GCRV-infected ScIRF3-overexpressing Ctenopharyngodon idellus kidney cells. These results indicate that ScIRF3 may play a role in the type I IFN immune response against GCRV in Squaliobarbus curriculus and can also inhibit GCRV replication in Ctenopharyngodon idellus kidney cells.
[Mh] Termos MeSH primário: Cyprinidae/imunologia
Doenças dos Peixes/imunologia
Proteínas de Peixes/imunologia
Fator Regulador 3 de Interferon/imunologia
Reoviridae/imunologia
[Mh] Termos MeSH secundário: Sequência de Aminoácidos
Animais
Cyprinidae/metabolismo
Cyprinidae/virologia
Doenças dos Peixes/metabolismo
Doenças dos Peixes/virologia
Proteínas de Peixes/classificação
Proteínas de Peixes/metabolismo
Perfilação da Expressão Gênica/métodos
Interações Hospedeiro-Patógeno/imunologia
Fator Regulador 3 de Interferon/genética
Fator Regulador 3 de Interferon/metabolismo
Interferon Tipo I/genética
Interferon Tipo I/imunologia
Interferon Tipo I/metabolismo
Filogenia
Reoviridae/fisiologia
Homologia de Sequência de Aminoácidos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Fish Proteins); 0 (Interferon Regulatory Factor-3); 0 (Interferon Type I)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180226
[Lr] Data última revisão:
180226
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180118
[St] Status:MEDLINE


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[PMID]:29317664
[Au] Autor:Choi HJ; Park A; Kang S; Lee E; Lee TA; Ra EA; Lee J; Lee S; Park B
[Ad] Endereço:Department of Systems Biology, College of Life Science and Biotechnology, Yonsei University, Seoul, 03722, South Korea.
[Ti] Título:Human cytomegalovirus-encoded US9 targets MAVS and STING signaling to evade type I interferon immune responses.
[So] Source:Nat Commun;9(1):125, 2018 01 09.
[Is] ISSN:2041-1723
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Human cytomegalovirus (HCMV) has evolved sophisticated immune evasion mechanisms that target both the innate and adaptive immune responses. However, how HCMV encoded proteins are involved in this immune escape is not clear. Here, we show that HCMV glycoprotein US9 inhibits the IFN-ß response by targeting the mitochondrial antiviral-signaling protein (MAVS) and stimulator of interferon genes (STING)-mediated signaling pathways. US9 accumulation in mitochondria attenuates the mitochondrial membrane potential, leading to promotion of MAVS leakage from the mitochondria. Furthermore, US9 disrupts STING oligomerization and STING-TBK1 association through competitive interaction. Intriguingly, US9 blocks interferon regulatory factor 3 (IRF3) nuclear translocation and its cytoplasmic domain is essential for inhibiting IRF3 activation. Mutant HCMV lacking US7-16 is impaired in antagonism of MAVS/STING-mediated IFN-ß expression, an effect that is reversible by the introduction of US9. Our findings indicate that HCMV US9 is an antagonist of IFN signaling to persistently evade host innate antiviral responses.
[Mh] Termos MeSH primário: Proteínas Adaptadoras de Transdução de Sinal/imunologia
Interferon Tipo I/imunologia
Glicoproteínas de Membrana/imunologia
Proteínas de Membrana/imunologia
Proteínas Virais/imunologia
[Mh] Termos MeSH secundário: Proteínas Adaptadoras de Transdução de Sinal/metabolismo
Células Cultivadas
Células HEK293
Células HeLa
Interações Hospedeiro-Patógeno/imunologia
Seres Humanos
Evasão da Resposta Imune/imunologia
Fator Regulador 3 de Interferon/imunologia
Fator Regulador 3 de Interferon/metabolismo
Interferon Tipo I/metabolismo
Glicoproteínas de Membrana/fisiologia
Proteínas de Membrana/metabolismo
Mitocôndrias/imunologia
Mitocôndrias/metabolismo
Mitocôndrias/virologia
Transdução de Sinais/imunologia
Células U937
Proteínas Virais/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Adaptor Proteins, Signal Transducing); 0 (IRF3 protein, human); 0 (Interferon Regulatory Factor-3); 0 (Interferon Type I); 0 (MPYS protein, human); 0 (Membrane Glycoproteins); 0 (Membrane Proteins); 0 (US9 protein, Human herpesvirus 5); 0 (VISA protein, human); 0 (Viral Proteins)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180226
[Lr] Data última revisão:
180226
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180111
[St] Status:MEDLINE
[do] DOI:10.1038/s41467-017-02624-8


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[PMID]:29324751
[Au] Autor:Echebli N; Tchitchek N; Dupuy S; Bruel T; Peireira Bittencourt Passaes C; Bosquet N; Le Grand R; Bourgeois C; Favier B; Cheynier R; Lambotte O; Vaslin B
[Ad] Endereço:CEA, Université Paris Sud, INSERM U1184, Immunology of Viral Infections and Autoimmune Diseases (IMVA), IDMIT Department / IBFJ, Fontenay-aux-Roses, France.
[Ti] Título:Stage-specific IFN-induced and IFN gene expression reveal convergence of type I and type II IFN and highlight their role in both acute and chronic stage of pathogenic SIV infection.
[So] Source:PLoS One;13(1):e0190334, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Interferons (IFNs) play a major role in controlling viral infections including HIV/SIV infections. Persistent up-regulation of interferon stimulated genes (ISGs) is associated with chronic immune activation and progression in SIV/HIV infections, but the respective contribution of different IFNs is unclear. We analyzed the expression of IFN genes and ISGs in tissues of SIV infected macaques to understand the respective roles of type I and type II IFNs. Both IFN types were induced in lymph nodes during early stage of primary infection and to some extent in rectal biopsies but not in PBMCs. Induction of Type II IFN expression persisted during the chronic phase, in contrast to undetectable induction of type I IFN expression. Global gene expression analysis with a major focus on ISGs revealed that at both acute and chronic infection phases most differentially expressed ISGs were inducible by both type I and type II IFNs and displayed the highest increases, indicating strong convergence and synergy between type I and type II IFNs. The analysis of functional signatures of ISG expression revealed temporal changes in IFN expression patterns identifying phase-specific ISGs. These results suggest that IFN-γ strongly contribute to shape ISG upregulation in addition to type I IFN.
[Mh] Termos MeSH primário: Expressão Gênica
Interferon Tipo I/genética
Interferon gama/genética
Síndrome de Imunodeficiência Adquirida dos Símios/imunologia
[Mh] Termos MeSH secundário: Doença Aguda
Animais
Doença Crônica
Macaca fascicularis
Vírus da Imunodeficiência Símia/imunologia
Vírus da Imunodeficiência Símia/fisiologia
Transcriptoma
Replicação Viral
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Interferon Type I); 82115-62-6 (Interferon-gamma)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180223
[Lr] Data última revisão:
180223
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180112
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0190334


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[PMID]:29293661
[Au] Autor:Monson EA; Crosse KM; Das M; Helbig KJ
[Ad] Endereço:Department of Physiology, Anatomy and Microbiology, La Trobe University, Melbourne, Victoria.
[Ti] Título:Lipid droplet density alters the early innate immune response to viral infection.
[So] Source:PLoS One;13(1):e0190597, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The cellular localisation of many innate signalling events following viral infection has yet to be elucidated, however there has been a few cases in which membranes of certain cellular organelles have acted as platforms to these events. Of these, lipid droplets (LDs) have recently been identified as signalling platforms for innate TLR7 and 9 signalling. Despite their wide range of similar roles in various metabolic pathways, LDs have been overlooked as potential platforms for antiviral innate signalling events. This study established an in vitro model to evaluate the efficiency of the early innate immune response in cells with reduced LD content to the viral mimics, dsDNA and dsRNA, and Sendai viral infection. Using RT-qPCR, the expression of IFN-ß and IFN-λ was quantified following stimulation along with the expression of specific ISGs. Luciferase based assays evaluated the combined expression of ISRE-promoter driven ISGs under IFN-ß stimulation. Cellular LD content did not alter the entry of fluorescently labelled viral mimics into cells, but significantly decreased the ability of both Huh-7 and HeLa cells to produce type I and III IFN, as well as downstream ISG expression, indicative of an impeded innate immune response. This observation was also seen during Sendai virus infection of HeLa cells, where both control and LD reduced cells replicated the virus to the same level, but a significantly impaired type I and III IFN response was observed in the LD reduced cells. In addition to altered IFN production, cells with reduced LD content exhibited decreased expression of specific antiviral ISGs: Viperin, IFIT-1 and OAS-1 under IFN-ß stimulation; However the overall induction of the ISRE-promoter was not effected. This study implicates a role for LDs in an efficient early innate host response to viral infection and future work will endeavour to determine the precise role these important organelles play in induction of an antiviral response.
[Mh] Termos MeSH primário: Imunidade Inata
Gotículas Lipídicas/metabolismo
Viroses/imunologia
[Mh] Termos MeSH secundário: Western Blotting
Linhagem Celular
Meios de Cultura
Seres Humanos
Interferon Tipo I/imunologia
Ácidos Nucleicos/metabolismo
RNA de Cadeia Dupla/imunologia
Reação em Cadeia da Polimerase em Tempo Real
Vírus Sendai/patogenicidade
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Culture Media); 0 (Interferon Type I); 0 (Nucleic Acids); 0 (RNA, Double-Stranded)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180221
[Lr] Data última revisão:
180221
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180103
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0190597


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[PMID]:29180807
[Au] Autor:Chiang JJ; Sparrer KMJ; van Gent M; Lässig C; Huang T; Osterrieder N; Hopfner KP; Gack MU
[Ad] Endereço:Department of Microbiology and Immunobiology, Harvard Medical School, Boston, MA, USA.
[Ti] Título:Viral unmasking of cellular 5S rRNA pseudogene transcripts induces RIG-I-mediated immunity.
[So] Source:Nat Immunol;19(1):53-62, 2018 Jan.
[Is] ISSN:1529-2916
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The sensor RIG-I detects double-stranded RNA derived from RNA viruses. Although RIG-I is also known to have a role in the antiviral response to DNA viruses, physiological RNA species recognized by RIG-I during infection with a DNA virus are largely unknown. Using next-generation RNA sequencing (RNAseq), we found that host-derived RNAs, most prominently 5S ribosomal RNA pseudogene 141 (RNA5SP141), bound to RIG-I during infection with herpes simplex virus 1 (HSV-1). Infection with HSV-1 induced relocalization of RNA5SP141 from the nucleus to the cytoplasm, and virus-induced shutoff of host protein synthesis downregulated the abundance of RNA5SP141-interacting proteins, which allowed RNA5SP141 to bind RIG-I and induce the expression of type I interferons. Silencing of RNA5SP141 strongly dampened the antiviral response to HSV-1 and the related virus Epstein-Barr virus (EBV), as well as influenza A virus (IAV). Our findings reveal that antiviral immunity can be triggered by host RNAs that are unshielded following depletion of their respective binding proteins by the virus.
[Mh] Termos MeSH primário: Proteína DEAD-box 58/imunologia
Herpesvirus Humano 1/imunologia
Imunidade/imunologia
RNA Ribossômico 5S/imunologia
[Mh] Termos MeSH secundário: Animais
Células Cultivadas
Cercopithecus aethiops
Proteína DEAD-box 58/metabolismo
Expressão Gênica/imunologia
Células HEK293
Herpesvirus Humano 1/fisiologia
Interações Hospedeiro-Patógeno/imunologia
Seres Humanos
Interferon Tipo I/genética
Interferon Tipo I/imunologia
Interferon Tipo I/metabolismo
Camundongos Knockout
Pseudogenes/genética
Transporte de RNA/imunologia
RNA Ribossômico 5S/genética
RNA Ribossômico 5S/metabolismo
Células Vero
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Interferon Type I); 0 (RNA, Ribosomal, 5S); EC 3.6.1.- (DDX58 protein, human); EC 3.6.4.13 (DEAD Box Protein 58)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:180220
[Lr] Data última revisão:
180220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171129
[St] Status:MEDLINE
[do] DOI:10.1038/s41590-017-0005-y


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[PMID]:27771387
[Au] Autor:Alfaiate D; Lucifora J; Abeywickrama-Samarakoon N; Michelet M; Testoni B; Cortay JC; Sureau C; Zoulim F; Dény P; Durantel D
[Ad] Endereço:INSERM U1052, CNRS UMR-5286, Cancer Research Center of Lyon (CRCL), 69008 Lyon, France; University of Lyon, Université Claude-Bernard (UCBL), 69008 Lyon, France.
[Ti] Título:HDV RNA replication is associated with HBV repression and interferon-stimulated genes induction in super-infected hepatocytes.
[So] Source:Antiviral Res;136:19-31, 2016 12.
[Is] ISSN:1872-9096
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Hepatitis D virus (HDV) super-infection of Hepatitis B virus (HBV)-infected patients is the most aggressive form of viral hepatitis. HDV infection is not susceptible to direct anti-HBV drugs, and only suboptimal antiviral responses are obtained with interferon (IFN)-alpha-based therapy. To get insights on HDV replication and interplay with HBV in physiologically relevant hepatocytes, differentiated HepaRG (dHepaRG) cells, previously infected or not with HBV, were infected with HDV, and viral markers were extensively analyzed. Innate and IFN responses to HDV were monitored by measuring pro-inflammatory and interferon-stimulated gene (ISG) expression. Both mono- and super-infected dHepaRG cells supported a strong HDV intracellular replication, which was accompanied by a strong secretion of infectious HDV virions only in the super-infection setting and despite the low number of co-infected cells. Upon HDV super-infection, HBV replication markers including HBeAg, total HBV-DNA and pregenomic RNA were significantly decreased, confirming the interference of HDV on HBV. Yet, no decrease of circular covalently closed HBV DNA (cccDNA) and HBsAg levels was evidenced. At the peak of HDV-RNA accumulation and onset of interference on HBV replication, a strong type-I IFN response was observed, with interferon stimulated genes, RSAD2 (Viperin) and IFI78 (MxA) being highly induced. We established a cellular model to characterize in more detail the direct interference of HBV and HDV, and the indirect interplay between the two viruses via innate immune responses. This model will be instrumental to assess molecular and immunological mechanisms of this viral interference.
[Mh] Termos MeSH primário: Vírus da Hepatite B/fisiologia
Vírus Delta da Hepatite/fisiologia
Hepatócitos/virologia
Imunidade Inata
Interferons/imunologia
Interferência Viral
Replicação Viral
[Mh] Termos MeSH secundário: Células Cultivadas
Coinfecção
Replicação do DNA
DNA Circular
Hepatite B/virologia
Antígenos E da Hepatite B/genética
Hepatite D/virologia
Vírus Delta da Hepatite/genética
Seres Humanos
Interferon Tipo I/imunologia
Proteínas de Resistência a Myxovirus/genética
Proteínas/genética
RNA Viral/biossíntese
RNA Viral/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (DNA, Circular); 0 (Hepatitis B e Antigens); 0 (Interferon Type I); 0 (MX1 protein, human); 0 (Myxovirus Resistance Proteins); 0 (Proteins); 0 (RNA, Viral); 0 (RSAD2 protein, human); 9008-11-1 (Interferons)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:180213
[Lr] Data última revisão:
180213
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161107
[St] Status:MEDLINE


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[PMID]:29293082
[Au] Autor:Hernandez Reyes Y; Provost C; Traesel CK; Jacques M; Gagnon CA
[Ad] Endereço:Centre de recherche en infectiologie porcine et avicole (CRIPA) et Groupe de recherche sur les maladies infectieuses en production animale (GREMIP), Faculté de médecine vétérinaire, Université de Montréal, St-Hyacinthe, Québec, J2S 2M2, Canada.
[Ti] Título:Actinobacillus pleuropneumoniae culture supernatant antiviral effect against porcine reproductive and respiratory syndrome virus occurs prior to the viral genome replication and transcription through actin depolymerization.
[So] Source:J Med Microbiol;67(2):249-264, 2018 Feb.
[Is] ISSN:1473-5644
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:PURPOSE: Recently, the strong antiviral activity of an Actinobacillus pleuropneumoniae (App) culture supernatant against porcine reproductive and respiratory syndrome virus (PRRSV) was discovered. Following this finding, the objective of the present study was to understand how the App culture supernatant inhibits PRRSV replication in its natural targeted host cells, i.e. porcine alveolar macrophages (PAMs). METHODOLOGY: Several assays were conducted with App culture supernatant-treated PRRSV-infected cell lines, such as PAM, St-Jude porcine lung and MARC-145 cells. RT-qPCR assays were used to determine the expression levels of type I and II IFN mRNAs, viral genomic (gRNA) and sub-genomic RNAs (sgRNAs). Proteomic, Western blot and immunofluorescence assays were conducted to determine the involvement of actin filaments in the App culture supernatant antiviral effect.Results/Key findings. Type I and II IFN mRNA expressions were not upregulated by the App culture supernatant. Time courses of gRNA and sgRNA expression levels demonstrated that the App culture supernatant inhibits PRRSV infection before the first viral transcription cycle. Western blot experiments confirmed an increase in the expression of cofilin (actin cytoskeleton dynamics regulator) and immunofluorescence also demonstrated a significant decrease of actin filaments in App culture supernatant-treated PRRSV-infected PAM cells. App culture supernatant antiviral activity was also demonstrated against other PRRSV strains of genotypes I and II. CONCLUSION: App culture supernatant antiviral effect against PRRSV takes place early during PRRSV infection. Results suggest that App culture supernatant antiviral effect may take place via the activation of cofilin, which induces actin depolymerization and subsequently, probably affects PRRSV endocytosis. Other experiments are needed to fully validate this latest hypothesis.
[Mh] Termos MeSH primário: Actinobacillus pleuropneumoniae/fisiologia
Actinas/metabolismo
Antivirais/farmacologia
Vírus da Síndrome Respiratória e Reprodutiva Suína/fisiologia
Replicação Viral/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Antibiose
Linhagem Celular
Meios de Cultura/química
Genoma Viral
Interferon Tipo I/genética
Macrófagos Alveolares/efeitos dos fármacos
Macrófagos Alveolares/virologia
Vírus da Síndrome Respiratória e Reprodutiva Suína/genética
Reação em Cadeia da Polimerase em Tempo Real
Suínos
Transcrição Genética/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Actins); 0 (Antiviral Agents); 0 (Culture Media); 0 (Interferon Type I)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180206
[Lr] Data última revisão:
180206
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180103
[St] Status:MEDLINE
[do] DOI:10.1099/jmm.0.000659


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[PMID]:29281695
[Au] Autor:Lesage-Padilla A; Forde N; Poirée M; Healey GD; Giraud-Delville C; Reinaud P; Eozenou C; Vitorino Carvalho A; Galio L; Raliou M; Oudin JF; Richard C; Sheldon IM; Charpigny G; Lonergan P; Sandra O
[Ad] Endereço:UMR BDR, INRA, ENVA, Université Paris Saclay, Jouy en Josas, France.
[Ti] Título:Maternal metabolism affects endometrial expression of oxidative stress and FOXL2 genes in cattle.
[So] Source:PLoS One;12(12):e0189942, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Intensive selection for milk production has led to reduced reproductive efficiency in high-producing dairy cattle. The impact of intensive milk production on oocyte quality as well as early embryo development has been established but few analyses have addressed this question at the initiation of implantation, a critical milestone ensuring a successful pregnancy and normal post-natal development. Our study aimed to determine if contrasted maternal metabolism affects the previously described sensory properties of the endometrium to the conceptus in cattle. Following embryo transfer at Day 7 post-oestrus, endometrial caruncular (CAR) and intercaruncular (ICAR) areas were collected at Day 19 from primiparous postpartum Holstein-Friesian cows that were dried-off immediately after parturition (i.e., never milked; DRY) or milked twice daily (LACT). Gene quantification indicated no significant impact of lactation on endometrial expression of transcripts previously reported as conceptus-regulated (PLET1, PTGS2, SOCS6) and interferon-tau stimulated (RSAD2, SOCS1, SOCS3, STAT1) factors or known as female hormone-regulated genes (FOXL2, SCARA5, PTGS2). Compared with LACT cows, DRY cows exhibited mRNA levels with increased expression for FOXL2 transcription factor and decreased expression for oxidative stress-related genes (CAT, SOD1, SOD2). In vivo and in vitro experiments highlighted that neither interferon-tau nor FOXL2 were involved in transcriptional regulation of CAT, SOD1 and SOD2. In addition, our data showed that variations in maternal metabolism had a higher impact on gene expression in ICAR areas. Collectively, our findings prompt the need to fully understand the extent to which modifications in endometrial physiology drive the trajectory of conceptus development from implantation onwards when maternal metabolism is altered.
[Mh] Termos MeSH primário: Endométrio/metabolismo
Proteína Forkhead Box L2/genética
Estresse Oxidativo
[Mh] Termos MeSH secundário: Animais
Catalase/genética
Bovinos
Feminino
Expressão Gênica
Interferon Tipo I/fisiologia
Proteínas da Gravidez/fisiologia
Análise de Componente Principal
RNA Mensageiro/genética
Reação em Cadeia da Polimerase em Tempo Real
Superóxido Dismutase/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Forkhead Box Protein L2); 0 (Interferon Type I); 0 (Pregnancy Proteins); 0 (RNA, Messenger); 0 (trophoblastin); EC 1.11.1.6 (Catalase); EC 1.15.1.1 (Superoxide Dismutase)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180206
[Lr] Data última revisão:
180206
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171228
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0189942



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